Schistosoma japonicum scFv-IL18 fusion DNA ameliorates hepatic fibrosis in schistosomiasis-infected mice via improving local concentration of IL-18 in liver

XiYa, Wang; Zhou, Yun; Qimei, Feng; Zhang, Shuju; Tieqiu, Yin; Xu, Shisan; Xia, Ying-ding; Xu, Jin; Jin, Jing; Wang, Shiping

doi:10.1016/j.exppara.2013.05.002

Cited by 4 publications

(2 citation statements)

References 22 publications

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“…A few publications report that IL-18 has an anti-fibrotic effect. The expression of IL-18 in serum and liver tissue was induced by DNA vaccine of IL-18, reducing schistosome-associated liver fibrosis (SSLF) (116). IL-18 was transfected into S. japonicum-infected hepatocytes, and hepatocytes expressed IL-18.…”

Section: Il-18 In Fibrosismentioning

confidence: 99%

Inflammasomes and Fibrosis

et al. 2021

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Fibrosis is the final common pathway of inflammatory diseases in various organs. The inflammasomes play an important role in the progression of fibrosis as innate immune receptors. There are four main members of the inflammasomes, such as NOD-like receptor protein 1 (NLRP1), NOD-like receptor protein 3 (NLRP3), NOD-like receptor C4 (NLRC4), and absent in melanoma 2 (AIM2), among which NLRP3 inflammasome is the most studied. NLRP3 inflammasome is typically composed of NLRP3, ASC and pro-caspase-1. The activation of inflammasome involves both “classical” and “non-classical” pathways and the former pathway is better understood. The “classical” activation pathway of inflammasome is that the backbone protein is activated by endogenous/exogenous stimulation, leading to inflammasome assembly. After the formation of “classic” inflammasome, pro-caspase-1 could self-activate. Caspase-1 cleaves cytokine precursors into mature cytokines, which are secreted extracellularly. At present, the “non-classical” activation pathway of inflammasome has not formed a unified model for activation process. This article reviews the role of NLRP1, NLRP3, NLRC4, AIM2 inflammasome, Caspase-1, IL-1β, IL-18 and IL-33 in the fibrogenesis.

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Section: Il-18 In Fibrosismentioning

confidence: 99%

Inflammasomes and Fibrosis

et al. 2021

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“…Recently, liver fibrosis was viewed as a reversible process [2]. After years of prevention and treatment of schistosomiasis in China, the new cases of Schistosoma infection have declined significantly, but there are still thousands of patients suffering from schistosomiasis [3]. The main pathological change of schistosomiasis is the formation of granuloma around the eggs of Schistosoma japonicum ( S .…”

Section: Introductionmentioning

confidence: 99%

Soluble Egg Antigens of Schistosoma japonicum Induce Senescence of Activated Hepatic Stellate Cells by Activation of the FoxO3a/SKP2/P27 Pathway

et al. 2016

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BackgroundLiver fibrosis was viewed as a reversible process. The activation of hepatic stellate cells (HSCs) is a key event in the process of liver fibrosis. The induction of senescence of HSCs would accelerate the clearance of the activated HSCs. Previously, we demonstrated that soluble egg antigens (SEA) of Schistosoma japonicum promoted the senescence of HSCs via STAT3/P53/P21 pathway. In this paper, our study was aimed to explore whether there are other signaling pathways in the process of SEA-induced HSCs aging and the underlying effect of SKP2/P27 signal on senescent HSCs.Methodology/Principal findingsHuman hepatic stellate cell line, LX-2 cells, were cultured and stimulated with SEA. Western blot and cellular immunofluorescence analysis were performed to determine the expression of senescence-associated protein, such as P27, SKP2 and FoxO3a. Besides, RNA interfering was applied to knockdown the expression of related protein. The senescence of HSCs was determined by senescence-associated β-gal staining. We found that SEA increased the expression of P27 protein, whereas it inhibited the expression of SKP2 and FoxO3a. Knockdown of P27 as well as overexpression of SKP2 both suppressed the SEA-induced senescence of HSCs. In addition, the nuclear translocation of FoxO3a from the nucleus to the cytoplasm was induced by SEA stimulation.Conclusions/SignificanceThe present study demonstrates that SEA promotes HSCs senescence through the FoxO3a/SKP2/P27 pathway.

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Anti-parasitic Antibodies from Phage Display

Goulart

Ribeiro

Costa-Cruz

2017

Recombinant Antibodies for Infectious Diseases

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Parasite infections affect billions of people and their domesticated animals worldwide, and remain as a significant cause of morbidity and mortality, but such diseases are still neglected in endemic countries. Therapeutic interventions consisted mostly of drugs, which are highly toxic and may lead to resistance. The immunopathology of parasites is very complex due to their multistage life cycles and long lifetime involving several hosts, leading many times to chronic infections and sometimes to death, by compromising nutritional status, affecting cognitive processes, and inducing severe tissue reactions. Vaccination is a challenge, and immunotherapy is completely disregarded because of their complex interactions with hosts and vectors. This review will bring concepts of immunological aspects for some important parasitic infections, and present the most recent phage display-derived antibodies or peptidomimetics for parasite targets. This chapter will also discuss the future perspectives of such potential anti-infective immunobiologicals for parasitic diseases.

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Schistosoma japonicum scFv-IL18 fusion DNA ameliorates hepatic fibrosis in schistosomiasis-infected mice via improving local concentration of IL-18 in liver

Cited by 4 publications

References 22 publications

Inflammasomes and Fibrosis

Inflammasomes and Fibrosis

Soluble Egg Antigens of Schistosoma japonicum Induce Senescence of Activated Hepatic Stellate Cells by Activation of the FoxO3a/SKP2/P27 Pathway

Anti-parasitic Antibodies from Phage Display

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